The purpose of this study is to test a biobehavorial model that implicates the hemodynamic patterns of behaviorally-evoked blood pressure responses in the pathogenesis of hypertension and concentric left ventricular hypertrophy. Sympathetic nervous system function will be evaluated extensively, as it is postulated to contribute to race and gender differences in the hemodynamic patterns of blood pressure regulation. The results of these studies should emphasize the importance of race and gender in prescribing pharmacological and/or behavioral treatment for hypertensive heart disease. Specific hypotheses under test fall into two general categories. The first concerns cardiac structural consequences. LVH (an increase in left ventricular mass) and concentric remodelling (an increase in the ratio of left ventricular wall thickness to chamber dimensions) are adaptations of the heart in response to increased afterload. Though blood pressure provides a convenient index of afterload, an abnormally high vascular resistance associated with a given blood pressure is more likely to promote the development of concentric LVH. Four hypotheses will be tested. In hypothesis #1a,we predict that high total peripheral resistance (TPR) levels during stress will be directly related to the degree of concentric remodelling in borderline hypertensives; and even in normotensives, a high relative wall thickness will be present in individuals who exhibit abnormally high levels of TPR during stress. In hypothesis 1b, we predict that TPR hyperreactivity will be more prevalent in black compared to white subjects and will predict racial differences in left ventricular structure, evident in normotensives as well as borderline hypertensives. In hypothesis 1c, we predict that premenopausal females compared to males will exhibit lower blood pressure and TPR responses during stress and these gender differences will predict gender differences in left ventricular structure. In hypothesis 1d, we predict that postmenopausal women will show increased systemic vascular resistance during stress compared to premenopausal women. Higher systemic vascular resistance responses during stress will be associated with concentric LV remodeling in postmenopausal compared to premenopausal women. The second general category concerns sympathetic nervous system mechanisms. Hemodynamic response patterns are determined by sympathetic activation and by the responsiveness of a and b adrenergic receptors in the cardiovascular system. Sympathetic nervous system activity, which reciprocally modulates adrenergic receptor responsiveness, is thought to play a pivotal role in the pathophysiology of the early stages of hypertensive disease. Four hypotheses will be tested. In hypothesis 2a, we predict that Black men will show greater vasoconstriction during stress than white men, which will be associated with heightened vascular a-adrenergic receptor responsiveness; whereas white men will show greater cardiac output reactivity than black men, which will be associated with greater epinephrine levels. In hypothesis 2b, we predict that White borderline hypertensive subjects will show greater cardiac output and systolic pressure reactivity than normotensives, which will be associated with enhanced epinephrine reactivity but attenuated b-adrenergic receptor responsiveness, indicative of b-receptor down-regulation; whereas black borderline hypertensives will show greater vasoconstriction during stress, which will be associated with heightened a-adrenergic receptor responsiveness in the absence of b-receptor down regulation. In hypothesis 2c, we predict that premenopausal white females will show lesser systolic pressure and stroke volume increases and lesser vascular reactivity than white males, which will be associated with lower epinephrine levels and lesser a-adrenergic receptor responsiveness. Lastly, in hypothesis 2d, we predict that increased vascular resistance in postmenopausal compared to premenopausal women will be associated with reduced responsiveness of vascular b2 receptors.